期刊
OSTEOARTHRITIS AND CARTILAGE
卷 16, 期 10, 页码 1205-1212出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.joca.2008.01.013
关键词
Chondrocytes; Glucosamine; Curcumin; Diacerein; Chondroprotection; qPCR
资金
- Department of Pharmaceutical Technology and Biopharmaceutics
- University of Vienna, Austria
- Integrated Project CellProm [NMP4-CT-2004-500039]
- European Community. Dr Goldring's [R01-AG022021]
Objective: To compare the effects of glucosamine (GlcN), curcumin, and diacerein in immortalized human C-28/12 chondrocytes at the cellular and the gene expression level. This study aimed to provide insights into the proposed beneficial effects of these agents and to assess the applicability of the C-28/12 cell line as a model for the evaluation of chondroprotective action. Methods: Interleukin-1 beta (IL-1 beta)-stimulated C-28/12 cells were cultured in the presence of GlcN, curcumin, and diacerein prior to the evaluation of parameters such as viability, morphology and proliferation. The impact of GlcN, curcumin, and diacerein on gene expression was determined using quantitative real-time RT-PCR (qPCR). Results: At the transcriptional level, 5 mM GlcN and 50 mu M diacerein increased the expression of cartilage-specific genes such as aggrecan (AGC) and collagen type II (COL2), while reducing collagen type I (COL1) mRNA levels. Moreover, the IL-1 beta-mediated shift in gene expression pattern was antagonized by GlcN and dacerein. These effects were associated with a significant reduction in cellular proliferation and the development of chondrocyte-specific cell morphology. In contrast, curcumin was not effective at lower concentrations but even damaged the cells at higher amounts. Conclusions: Both GlcN and diacerein promoted a differentiated chondrocytic phenotype of immortalized human C-28/12 chondrocytes by altering proliferation, morphology, and COL2/COL1 mRNA ratios. Moreover, both agents antagonized inhibitory effects of IL-1 beta by enhancing AGC and COL2 as well as by reducing COL1 mRNA levels. (C) 2008 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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